van der Vusse G J, Stam H
Dept. of Physiology, Medical Faculty Maastricht, University of Limburg, The Netherlands.
Basic Res Cardiol. 1987;82 Suppl 1:149-53. doi: 10.1007/978-3-662-08390-1_18.
Ischaemia has profound effects on myocardial metabolism and cell function in general. High energy phosphate and glycogen stores are depleted. Lactate, inorganic phosphate and hydrogen ions accumulate, exerting negative effects on the initially accelerated glycolytic flux. Fatty acid oxidation is inhibited. The cellular content of lipid intermediates, such as hydroxy-fatty acids, acyl CoA and acylcarnitine, increases in low-flow ischaemia hearts. Non-esterified fatty acid (NEFA) accumulation occurs after 30-60 min ischaemia. Endogenous triacylglycerol and phosphoglyceride turnover is most likely impaired, ultimately resulting in accumulation of lipid droplets in the oxygen deprived cells and in degradation of myocardial membranes. Accumulated lipid substances such as NEFA, acyl CoA, acylcarnitine and lysophosphoglycerides, are likely to be involved in the mechanism underlying ischaemia-induced damage to myocardial cells.
一般来说，缺血对心肌代谢和细胞功能有深远影响。高能磷酸和糖原储备耗竭。乳酸、无机磷酸和氢离子蓄积，对最初加速的糖酵解通量产生负面影响。脂肪酸氧化受到抑制。在低流量缺血心脏中，脂质中间体如羟基脂肪酸、酰基辅酶A和酰基肉碱的细胞含量增加。缺血30 - 60分钟后出现非酯化脂肪酸（NEFA）蓄积。内源性三酰甘油和磷酸甘油酯周转很可能受损，最终导致缺氧细胞中脂滴蓄积以及心肌膜降解。蓄积的脂质物质如NEFA、酰基辅酶A、酰基肉碱和溶血磷脂酰甘油可能参与缺血诱导心肌细胞损伤的机制。
